Under certain conditions of hypo- and hyperbaric decompression, gas-supersaturation of tissues and blood can cause bubbles to form there with serious medical consequences. The growing use of dysbaric environments by man has made this problem of decompression sickness increasingly important. The objective of the present physiological study is to increase the understanding of the early etiology of decompression sickness, an area which has received relatively little attention in the past. Essential information is lacking as to where and how the bubles form, and the factors which cause the dramatic lowering of liquid cavitation stability in vivo are still to be established. During the past phase of our study, some much needed information was obtained on gas bubble nucleation in solutions and interface systems in vitro as well as in microorganisms. During the next phase, several basic aspects of bubble formation in living systems will be examined, using various unicellular and multicellular organisms, biological fluids and blood cells. We will attempt to determine for example: (a) if gaseous nuclei commonly exist in organisms, (b) if spontaneous bubble nucleation can occur at gas-supersaturations that normally lead to in vivo bubbles, (c) the principal cause(s) of the apparent decrease in gas-supersaturation tolerance with increasing morphological complexity, and (d) the conditions for intracellular bubble nucleation. The methods to be used include microscopic observations and cinemicrographic recordings of events during decompression while manipulating the gas saturations and the rates of compression and have been developed. The results obtained will be used to formulate new approaches and to reevalutate existing concepts relating to formation of bubbles in vivo. Our long-range goal is to aid in the prevention and treatment of decompression sickness by contributing to the development of better hyperbaric gas mixtures, decompression procedures and pharmacological agents.